Ranolazine efficiency in hypertrophyc cardiomyopathy

Abstract

Hypertrophic cardiomyopathy (HCM) is a leading cause of sudden cardiovascular death that develops usually due to ventricular arrhythmia and a heart failure-related death dysfunction (Coleman J.A. et al., 2024). Ranolazine is an inhibitor of the late inward sodium current (IₙₐL). In HCM, several pathophysiologic features may make this mechanism relevant: enhanced late IₙₐL has been documented in human HCM cardiomyocytes (Coppini R., 2017). Diastolic dysfunction, increased wall stiffness, microvascular dysfunction and arrhythmogenic substrate are prominent in HCM – so a drug that might mitigate calcium overload, improve relaxation or reduce arrhythmias has theoretical appeal (Efthimiadis G.K., 2016).